Skeletal muscle loss in a subject due to age-, inactivity-, or disease-related disorders may have a negative impact on the overall health and well being of the subject. For example, skeletal muscle loss may lead to weakness, frailty, further muscle loss, susceptibility to injury, a decrease in the ability or desire to exercise, and so forth in the subject. Typically, skeletal muscle loss is regulated by two separate pathways: (1) decreased muscle protein synthesis and (2) increased muscle protein degradation. Together, these pathways generally accelerate and promote rapid muscle loss. Individually, each pathway on its own promotes skeletal muscle loss. Thus, inhibiting or preventing each pathway, individually or together, will have a mitigating effect on skeletal muscle loss.
With respect to the second pathway, age disorders (as evidenced by sarcopenia), disease disorders (as evidenced by cachexia), or general inactivity disorders (e.g., muscle wasting or atrophy due to lack of use or immobilization) may increase or upregulate muscle protein degradation. Thus, the loss of skeletal muscle attributable to age, inactivity, or disease may be mitigated by inhibiting, i.e., decreasing or preventing, muscle protein degradation.